کد مقاله | کد نشریه | سال انتشار | مقاله انگلیسی | نسخه تمام متن |
---|---|---|---|---|
4337988 | 1614833 | 2013 | 8 صفحه PDF | دانلود رایگان |
• Ataxin-3 protects cells against H2O2-induced oxidative stress.
• Ataxin-3 directly binds to Bcl-XL.
• The N-terminus of ataxin-3 interacts with the C-terminus of Bcl-XL.
• Ataxin-3 enhances the interaction between Bcl-XL and Bax.
Spinocerebellar ataxia type 3 (SCA3) is a neurodegenerative disorder associated with polyglutamine (polyQ) protein ataxin-3. Ataxin-3 is a multi-functional protein, but the precise mechanisms underlying the cellular functions of ataxin-3 remain to be elucidated. Here we demonstrate that ataxin-3 plays a protective role against cellular oxidative stress induced by H2O2 in a Bcl-XL-dependent manner. Ataxin-3 directly interacts with Bcl-XL. The N-terminus of ataxin-3 and the C-terminus of Bcl-XL are essential for the interaction. Ataxin-3 promotes the interaction between Bcl-XL and Bax, but does not affect the ubiquitination and degradation of Bcl-XL. Our data suggest that ataxin-3 plays an important role in regulating the Bcl-XL–Bax-mediated anti-oxidative response by modulating the interaction between Bcl-XL and Bax.
Journal: Neuroscience - Volume 243, 23 July 2013, Pages 14–21